The brachial plexus is a large cluster of nerves that passes from the spinal cord through the neck and the upper chest to the shoulder and arm. To reach the arm, the brachial plexus must pass through at least three anatomic tunnels. The main blood supply to and from the arm is provided by the subclavian artery and the subclavian vein, respectively. These major blood vessels pass through the same anatomic tunnels as the brachial plexus. Thoracic Outlet Syndrome (TOS) is a complex of signs and symptoms that results from narrowing of these tunnels and compression of one or more of these vital structures. TOS can be divided into three primary types:                Neurogenic Thoracic Outlet Syndrome: Neurogenic TOS is a compressive and entrapment neuropathy in which one or more of these tunnels becomes narrow, creating mechanical compression on the brachial plexus and/or altering its blood supply. This compression and altered blood flow result in pain, abnormal sensation, weakness, and eventual loss of muscle function in the affected areas.        Arterial Thoracic Outlet Syndrome: Arterial TOS results from mechanical compression of the subclavian or axillary artery, which causes arterial stenosis, post-stenotic aneurysm formation, and intramural thrombus formation. These changes result in decreased blood flow to the arm and/or embolism of thrombus to distal vessels, with pain, weakness, coldness and loss of pulse in the affected arm.        Venous Thoracic Outlet Syndrome: Venous TOS results from mechanical compression of the subclavian or axillary vein, which causes occlusive or non-occlusive thrombosis of the vein, damage to the lining of the vein, and eventual stricture formation that persists despite resolution of the extrinsic mechanical compression. These changes result in swelling, cyanosis, pain and altered function of the affected arm.        
The causative mechanisms for all three types of primary TOS are nearly identical, and compression of one vital structure is often accompanied by compression of the other vital structures in varying degrees. Therefore, each primary type of TOS described above frequently includes a component of one or both of the other two types of TOS.
Thoracic Outlet Syndrome occurs when two conditions are met:                The patient has anatomic predispositions or anomalies. These can include abnormal muscles or fibrous bands, exaggeration or distortion of the usual shapes of the chest and shoulder girdle bony structures, anomalous courses of the nerves that make up the brachial plexus, or anomalous arteries or veins that pass through the thoracic outlet.        The patient has a superimposed traumatic event or repetitive overuse syndrome that:                    Alters the soft tissues or bony structures that make up the anatomic tunnels, or            That causes direct injury to the brachial plexus, arteries, veins or soft tissues and bony structures that make up the anatomic tunnels, or            That alters the posture and position of the neck and shoulder girdle, leading to narrowing of the anatomic tunnels through which the brachial plexus, arteries and veins pass.                        
Neurogenic TOS is a compressive and entrapment neuropathy that has been clinically recognized for over one hundred years. Physicians frequently find these patients' cases complex and challenging. Patients often have a slowly-evolving course, experiencing symptoms intermittently early in the course of the disease and often only being symptomatic with the arms and neck in certain positions. As the disease progresses, the patients experience symptoms continuously, regardless of the position of their arms and neck. Patients often experience sensory changes early in the course of the disease, followed by vague muscle aching as the disease progresses. Eventually, patients experience muscle weakness, which in the late stages becomes evident as muscle atrophy and wasting, if the correct diagnosis is not made and definitive treatment is not undertaken. Unfortunately, when the disease progresses to this extent, muscle weakness and atrophy are unlikely to improve, even with definitive treatment.
Arterial TOS is frequently associated with an anomalous extra rib in the lower cervical spine, and was the first clinical form of TOS to be recognized, beginning with a case described in England in 1821, followed by a surgically proven case in 1861. It often has a dramatic clinical presentation due to either decreased blood flow to the affected arm or to the sudden development of blood clots embolizing to the distal vessels of the arm, causing gangrene. In this setting, the diagnosis is readily made. However, early diagnosis is critical to prevent the occurrence of these potentially serious complications.
Venous TOS frequently occurs in patients with an occupation requiring repetitive and/or strenuous use of their upper extremities, and is known by several other names, including effort thrombosis and Paget-Schroetter syndrome. It often has a dramatic clinical presentation due to swelling of the affected arm, decreased blood flow or loss of function. In addition, these patients are at risk of pulmonary embolism and pulmonary hypertension, either of which may be fatal. In this setting, the diagnosis is readily made. However, early diagnosis is critical to prevent the occurrence of potentially serious thromboembolic events, and to prevent permanent damage to the compressed vein, which predisposes the patient to repeated episodes of thrombosis formation and symptoms even after the mechanical compression of the vein has been treated.
Clinical, electrophysiologic and imaging tests have been developed over the past century, but none have been widely accepted as a gold standard for the diagnosis of TOS. Clinical tests utilize various positions of the patient's neck and arms while the pulse is palpated at the wrist. These tests have been shown to have a high number of false positive and false negative results. Electrophysiological tests are used to rule out the presence of other compressive and entrapment neuropathies of the upper extremity, but cannot confirm or rule out the diagnosis of TOS. Imaging tests have been used to evaluate the anatomy and pathology in patients with TOS. These tests have changed as the technology has evolved to allow more refined evaluation of anatomy and pathology in patients with TOS.
Since the 1960's, contrast angiography or venography has been performed to evaluate the arteries or veins of the arms, respectively, with the patient's arms placed in various provocative positions. This method duplicates the clinical tests in which the patient's pulse is palpated as their arms are moved into symptomatic positions. Angiography and venography are limited to evaluation of the compressed arteries and veins, but do not evaluate the abnormal anatomic tunnels that are causing this compression. Since the 1980's, CT scanning has been performed to evaluate the bony structures that border the thoracic outlet, or the arteries and veins of the arms, with the patient's arms placed in various provocative positions. CT scanning can also be performed with the patient's arms by their sides, allowing evaluation of the changes in the bony anatomic tunnels that occur with arm motion, and the resulting effects on the accompanying arteries or veins. CT scanning is limited in its evaluation of soft tissues, with inadequate differentiation of muscles and nerves in the thoracic outlet. Since the early 1990s, MRI scanning has been performed for the evaluation of soft tissue structures in the thoracic outlet, including the nerves of the brachial plexus, the arteries and veins of the arm, or the muscles that border the anatomic tunnels through which these vital structures pass to reach the arm. Like CT scanning, MRI scanning can be performed with the patient's arms placed in various provocative positions.
Each of these imaging tests has focused on one component of TOS, evaluating the bony structures, soft tissues, arteries, veins, or nerves. To date, there has been no single process that evaluates comprehensively the nerves, arteries and veins that pass through the thoracic outlet, the muscles and bony structures that form the anatomic tunnels of the thoracic outlet, the changes in the thoracic outlet that occur on arm movement, and the resulting effects of these changes on the brachial plexus, arteries and veins as they pass through these tunnels. The invention technique accomplishes these goals.